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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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The growth and maintenance of bone are regulated by a combination of nutritional factors, including vitamins, such as vitamin A, B12, C, D, and K.
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Author Spotlight: Integrating Traditional Chinese Medicine with Modern Pharmacology and Genomics for Assessing Postmenopausal Osteoporosis in Mice
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[Osteoporosis].

Brigitte Uebelhart1, Serge Ferrari1

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This summary is machine-generated.

Denosumab reduced fracture incidence after romosozumab treatment. However, stopping denosumab causes bone loss and fracture risk, while abaloparatide shows promise for fracture prevention.

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Area of Science:

  • Orthopedics
  • Endocrinology
  • Pharmacology

Background:

  • Osteoporosis treatment involves medications to reduce fracture risk.
  • Understanding drug sequencing and cessation effects is crucial for long-term bone health.
  • Specific patient populations, like those with diabetes, face unique fracture risks.

Purpose of the Study:

  • To evaluate the fracture incidence following denosumab treatment after prior romosozumab therapy.
  • To investigate the consequences of denosumab cessation on bone resorption and density.
  • To review the efficacy and safety of other osteoporosis medications like abaloparatide and the discontinued odanacatib.

Main Methods:

  • Comparative analysis of fracture incidence in patients treated with denosumab post-romosozumab versus placebo.
  • Observational assessment of bone turnover markers, bone mineral density, and fracture events after denosumab discontinuation.
  • Review of clinical trial data for abaloparatide and safety reports for odanacatib.

Main Results:

  • Denosumab treatment following romosozumab resulted in lower fracture incidence compared to placebo.
  • Cessation of denosumab led to a rebound in bone resorption, decreased bone mineral density, and an elevated risk of vertebral fractures.
  • Abaloparatide demonstrated a reduction in vertebral and non-vertebral fractures.
  • Odanacatib, a cathepsin K inhibitor, will not be available due to safety concerns.

Conclusions:

  • Sequential therapy with denosumab after romosozumab may be effective in reducing fractures.
  • Denosumab cessation poses significant risks requiring careful management strategies.
  • Abaloparatide represents a viable option for fracture prevention.
  • Bone quality alterations in diabetic patients contribute to increased fracture risk.